Time course of release of atrial natriuretic peptide in the anaesthetized dog

Abstract

In 12 chloralose anaesthetized dogs plasma concentration of immunoreactive atrial natriuretic peptide (IR-ANP) was measured using a radioimmunoassay. Plasma IR-ANP was 74 +/- 4.8 pg/mL (mean +/- SE) and increased by 39 +/- 4.1 pg/mL when left atrial pressure was increased by 10 cm H2O during partial mitral obstruction. Observation of the time course of the changes in IR-ANP during atrial distension showed that IR-ANP was increased within 2 min of atrial distension and declined after atrial distension, with a half-time of 4.5 min. The time course of the changes in IR-ANP was unaffected by vagotomy or administration of atenolol. Maximum electrical stimulation of the right ansa subclavia failed to produce any change in IR-ANP. IR-ANP was higher in coronary sinus plasma than in femoral arterial plasma confirming that the heart was the source of the IR-ANP. The results support the hypothesis that IR-ANP is released from the heart by a direct effect of stretch of the atrial wall rather than by a neural or humoral mechanism involving a reflex from atrial receptors.

Release of atrial natriuretic peptide from the isolated, blood-perfused right atrium of the dog.

“…On the other hand, plasma ANP concentration of the arterial blood of the donor dog (ANP-D), which perfused simul taneously both the right atrium (RA) and papillary muscle (PM) preparations, was about 100 pg/ml. The ANP D, the ANP con centration of the circulating blood of our donor dogs, was slightly higher than, but within the range of, circulating plasma ANP concentrations previously reported in dogs (7)(8)(9)(10)12). According to Ledsome et al (7,8), the plasma concentration of ANP in coronary sinus blood was only about 1.5 to 2 times higher than in arterial blood.…”

“…The ANP D, the ANP con centration of the circulating blood of our donor dogs, was slightly higher than, but within the range of, circulating plasma ANP concentrations previously reported in dogs (7)(8)(9)(10)12). According to Ledsome et al (7,8), the plasma concentration of ANP in coronary sinus blood was only about 1.5 to 2 times higher than in arterial blood. In our present experiments, plasma ANP concen tration of venous blood from the atrium (AN P A) was about 15 times higher than in arterial blood (ANP-D), suggesting that the ANP was directly released from the right atrium.…”

“…Elevated atrial pressure during atrial tachy cardia (5,18) and/or atrial frequency per se (19) have been proposed to be responsible for the increase in ANP release. In any case, there has been little direct and quantitative data for the ANP released from the atria into circulation, even though a number of reports on circulating plasma ANP concentration have been presented (5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18). right atrium.…”

Reduction of atrial natriuretic factor circulating levels by endogenous sympathetic activation in hypertensive patients.

“…'8 It is not clear to date whether factors other than atrial wall tension may be involved in the control of ANF release. In this regard, it has been shown that several hormonal agents,'8 [19][20][21][22] cardiac nerve activity, 8 and heart rate23 may also contribute to regulate ANF secretion. With regard to the possible influence of sympathetic nervous system on ANF release, the administration of pharmacologic doses of catecholamines has been shown to increase ANF levels,9' 21 but this effect could be explained by concurrent increases in atrial pressures.…”

Light- and electron-microscopic investigation of ANP-like immunoreactivity in aorta, carotid artery and cultured cardiac myocytes of the rat.

“…Atrial distension seems to be the major stimulus for the release of ANP by atrial myocytes (11,13,16,20,22,27). Immunohistochemical studies revealed ANP-like immunoreactivity in some extra-cardiac organs as salivary glands (2), sweat glands (28), central nervous system (10,12,23,25), adrenal medulla and sympathetic ganglia (9), venae cavae and pulmonary veins (15,26,31).…”